Cytotoxic T cells recognize complexes between major histocompatibility complex (MHC) class I molecules and specific antigen peptides (foreign substances), and are thereby activated to exert cytotoxic activity against target cells. In contrast, natural killer (NK) cells typically damage target cells expressing no MHC class I molecules. The expression of such MHC class I molecules on normal cell surface is suppressed by viral infection or canceration. NK cells exert cytotoxic activity against such abnormal cells with decreased MHC class I molecule expression levels. It is therefore thought that NK cells play a central role in the innate immunity mechanism by eliminating cancerated cells or cells infected with viruses. NK cells were in fact identified as cells having the activity of spontaneously damaging certain cancer cells (see Non-Patent Document 1). Furthermore, such in vivo roles of NK cells are supported by the disease called Chediak-Higashi syndrome, which is caused by a deficiency in NK cell activity (Chediak-Higashi syndrome is due to a chromosome abnormality and enters the advanced stage when the patient is over 10 years old, making it impossible to control viral infection, and resulting in malignant lymphoma-like pathological changes and death by pancytopenia after 2 to 3 months).
Recently, transgenic mice lacking NK1.1+CD3-cells (NK cells) were generated. Analyses of their characteristics revealed that: NK cells    (i) play an important role in suppressing metastasis and growth of cancer cells; and    (ii) are major producers of interferon (IFN) γ in response to bacterial endotoxins (see Non-Patent Document 2).
Meanwhile, it has recently been found that a fourth lymphocyte, NKT cell, that has a NK cell receptor as well as an identical T cell receptor and characteristics of both innate and acquired immunities, are distributed in a wide variety of organs, including liver and bone marrow. In addition, these cells have been found to be involved in immunotolerance, and in many diseases such as autoimmune diseases, hepatitis, and infections. Based on studies using mice that develop multiple sclerosis early in life, it has been found that there is a certain relationship between NKT cells, which are immune cells included in lymphocytes, and the onset of multiple sclerosis (see Non-Patent Document 3). In addition, it has been suggested that asthma may be preventable by inactivating NKT cells, because no allergic airway hyperreactivity, which is a major asthma symptom, is detected in NKT-deficient mice (see Non-Patent Document 4). The revealed activation mechanism for NKT cells shows that unlike NK cells, NKT cells are activated through stimulation of the T cell receptor or through α-galactosylceramide (α-GalCer), which is a glucolipid presented to the CD1d receptor on dendritic cells (see Non-Patent Document 3). Meanwhile, like NK cells, NKT cells exert cytotoxic activity against cells with decreased MHC class I molecule expression levels, and is therefore thought to regulate cytotoxic activity by almost the same mechanism as the killer cell inhibitory receptor (hereinafter abbreviated as “KIR”), which has been identified as an inhibitory regulator molecule involved in the cytotoxic activity of lymphocyte populations. However, NKT subsets that do not express known KIRs are also known to exist. In addition, much was unclear about signal cascades and inhibitory receptors that act negatively in the activation, necessitating further studies.
While ligand substances that are effective for NKT cell activation have been found, low-molecular-weight ligands that specifically activate NK cells are yet to be identified.    Non-Patent Document 1: Trinchieri G., Adv Immunol. (1989), 47, 187-376    Non-Patent Document 2: Sungjin Kim, Koho Iizuka, Hector L. Aguila, Irving L. Weissman, and Wayne M. Yokoyama, Proc. Natl. Acad. Sci. (2000), 97, 2731-2736    Non-Patent Document 3: Michishige Harada, Masaru Taniguchi, Protein, Nucleic acid, and Enzyme (Tanpakushitsu Kakusan Kouso) (2002), 47, 2109-2116    Non-Patent Document 4: Akbari O, Stock P, Meyer E, Kronenberg M, Sidobre S, Nakayama T, Taniguchi M, Grusby M J, DeKruyff R H, Umetsu D T, Nat. Med. (2003), 9, 582-588